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Intravenous Procaine Amide and Left Ventricular Performance
were available. As mentioned in a previous issue of Chest,' we attempted such a study with this same group of patients. Once again, the severity of their lung disease differentiates them from Dr. Baum's patients and prevented such a sham study. Without oxygen therapy, patients with this severity of hypoxemic obstructive airway disease were unable to tolerate a month at home and the "control" period ended with an episode of acute respiratory insufficiency.
A. lay Block, M.D. Chief, Pulmonary Division Associate Professor of Medicine and Anesthesiology University of Florida, Gainesville
no myocardial depressant effects. It is just that Jawad-Kanber and Sherrod have not clearly demonstrated such an effect with their data. I am not aware of any study which does document the effect of this drug on left ventricular contractility in intact, conscious patients. Rex MacAlpin, M.D. UCLA School of Medicine Los Angeles
1 Stafford RW, Harris WS, Weissler AM, et al: Systolic time intervals as indexes of gravitational circulatory stress in man. Am J Cardiol 19: 152, 1967
To the Editor: 1 Krop HD, Block AJ, Cohen E: Neuropsychological effects of continuous oxygen therapy in chronic obstructive pulmonary disease. Chest 64:317, 1973
Intravenous Procaine Amide and Left Ventricular Performance
The only message that the study tried to relay was that procaine amide could be given intravenously with some margin of safety; since a loading dose produced measurable decrease in pump performance and ventricular mechanics (peak dpldt), but not to a level that was clinically significant in terms of untoward symptoms or signs in the patient evaluated.
G. Jawad-Kanber,M.D., F.C.C.P. Oak Park, Zllimis
To the Editor: In their report of the effects of intravenous procaine arnide on left ventricular function (Chest 66: 269-272, 1974), Drs. Jawad-Kanber and Sherrod concluded that the hemodynamic alterations which they observed are consistent with a myocardial depression or a negative inotropic effect of the drug. I presume they based this conclusion on the observation of decreases in cardiac index, arterial pressure, left ventricular stroke work, and peak positive left ventricular dpldt. Also noted was a rise in rate corrected pre-ejection ~ e r i o d .It seems to me, however, that they failed to appreciate that none of these hemodynamic variables are direct measures of left ventricular contractility; in fact, their data are equally or more consistent with a reduction in venous return and a decline in left ventricular end-diastolic volume and fiber length. The fall in left ventricular end-diastolic and pulmonary arterial pressures that was observed would be consistent with this alternate hypothesis. It is well established that a reduction in left ventricular "preload" will result in decreases in stroke volume, stroke work, and peak dpldt, and this also will cause an increase in rate corrected pre-ejection period1 without any intrinsic change in contractile state of the myocardium. I do not wish to imply that procaine amide has CHEST, 67: 6, JUNE, 1975
Comment on Lung Biopsy Techniques To the Editor: In reference to the report entitled "Percutaneous Needle Biopsy of the Lung: Report of Two Fatal Complications" ( Chest 66:216-218, 1974 ), we would like to comment on the conclusions reached by Drs. Norenberg, Claxton, and Takaro on the use of different lung biopsy techniques. In the past five years at the Washington University Medical Center, a p proximately 125 cutting needle biopsies of the lung have been performed by seven different individuals. In five instances the patient died during or immediately after the procedure. Four of these patients had immediate massive hemoptysis as described by Dr. Norenberg and his colleagues. Another young man with sarcoidosis developed a permanent hemiparalysis after the procedure, presumably from air embolus. Because of these results, we no longer use this biopsy technique. Our experience with aspiration needle biopsy has been quite different. In over 300 cases we have had no deaths, with significant morbidity limited to COMMUNICATIONS TO THE EDITOR 737
A. lay Block, M.D. Chief, Pulmonary Division Associate Professor of Medicine and Anesthesiology University of Florida, Gainesville
no myocardial depressant effects. It is just that Jawad-Kanber and Sherrod have not clearly demonstrated such an effect with their data. I am not aware of any study which does document the effect of this drug on left ventricular contractility in intact, conscious patients. Rex MacAlpin, M.D. UCLA School of Medicine Los Angeles
1 Stafford RW, Harris WS, Weissler AM, et al: Systolic time intervals as indexes of gravitational circulatory stress in man. Am J Cardiol 19: 152, 1967
To the Editor: 1 Krop HD, Block AJ, Cohen E: Neuropsychological effects of continuous oxygen therapy in chronic obstructive pulmonary disease. Chest 64:317, 1973
Intravenous Procaine Amide and Left Ventricular Performance
The only message that the study tried to relay was that procaine amide could be given intravenously with some margin of safety; since a loading dose produced measurable decrease in pump performance and ventricular mechanics (peak dpldt), but not to a level that was clinically significant in terms of untoward symptoms or signs in the patient evaluated.
G. Jawad-Kanber,M.D., F.C.C.P. Oak Park, Zllimis
To the Editor: In their report of the effects of intravenous procaine arnide on left ventricular function (Chest 66: 269-272, 1974), Drs. Jawad-Kanber and Sherrod concluded that the hemodynamic alterations which they observed are consistent with a myocardial depression or a negative inotropic effect of the drug. I presume they based this conclusion on the observation of decreases in cardiac index, arterial pressure, left ventricular stroke work, and peak positive left ventricular dpldt. Also noted was a rise in rate corrected pre-ejection ~ e r i o d .It seems to me, however, that they failed to appreciate that none of these hemodynamic variables are direct measures of left ventricular contractility; in fact, their data are equally or more consistent with a reduction in venous return and a decline in left ventricular end-diastolic volume and fiber length. The fall in left ventricular end-diastolic and pulmonary arterial pressures that was observed would be consistent with this alternate hypothesis. It is well established that a reduction in left ventricular "preload" will result in decreases in stroke volume, stroke work, and peak dpldt, and this also will cause an increase in rate corrected pre-ejection period1 without any intrinsic change in contractile state of the myocardium. I do not wish to imply that procaine amide has CHEST, 67: 6, JUNE, 1975
Comment on Lung Biopsy Techniques To the Editor: In reference to the report entitled "Percutaneous Needle Biopsy of the Lung: Report of Two Fatal Complications" ( Chest 66:216-218, 1974 ), we would like to comment on the conclusions reached by Drs. Norenberg, Claxton, and Takaro on the use of different lung biopsy techniques. In the past five years at the Washington University Medical Center, a p proximately 125 cutting needle biopsies of the lung have been performed by seven different individuals. In five instances the patient died during or immediately after the procedure. Four of these patients had immediate massive hemoptysis as described by Dr. Norenberg and his colleagues. Another young man with sarcoidosis developed a permanent hemiparalysis after the procedure, presumably from air embolus. Because of these results, we no longer use this biopsy technique. Our experience with aspiration needle biopsy has been quite different. In over 300 cases we have had no deaths, with significant morbidity limited to COMMUNICATIONS TO THE EDITOR 737